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Syncytiotrophoblast of Placentae from Women with Zika Virus Infection Has Altered Tight Junction Protein Expression and Increased Paracellular Permeability
Open AccessArticle

The ZIKA Virus Delays Cell Death Through the Anti-Apoptotic Bcl-2 Family Proteins

PIMIT, Processus Infectieux en Milieu Insulaire Tropical, Université de La Réunion, INSERM UMR 1187, CNRS 9192, IRD 249, Plateforme CYROI, 97490 Sainte-Clotilde, Ile de La Réunion, France
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Cells 2019, 8(11), 1338; https://doi.org/10.3390/cells8111338
Received: 16 September 2019 / Revised: 22 October 2019 / Accepted: 26 October 2019 / Published: 29 October 2019
(This article belongs to the Special Issue Zika Virus and Host Interactions)
Zika virus (ZIKV) is an emerging human mosquito-transmitted pathogen of global concern, known to be associated with complications such as congenital defects and neurological disorders in adults. ZIKV infection is associated with induction of cell death. However, previous studies suggest that the virally induced apoptosis occurs at a slower rate compared to the course of viral production. In this present study, we investigated the capacity of ZIKV to delay host cell apoptosis. We provide evidence that ZIKV has the ability to interfere with apoptosis whether it is intrinsically or extrinsically induced. In cells expressing viral replicon-type constructions, we show that this control is achieved through replication. Finally, our work highlights an important role for anti-apoptotic Bcl-2 family protein in the ability of ZIKV to control apoptotic pathways, avoiding premature cell death and thereby promoting virus replication in the host-cell. View Full-Text
Keywords: Zika virus; apoptosis; viral replication; Bcl-2 protein family Zika virus; apoptosis; viral replication; Bcl-2 protein family
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Turpin, J.; Frumence, E.; Desprès, P.; Viranaicken, W.; Krejbich-Trotot, P. The ZIKA Virus Delays Cell Death Through the Anti-Apoptotic Bcl-2 Family Proteins. Cells 2019, 8, 1338.

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